Intracranial empyema: literature review and two novel cases in cats.

OBJECTIVES: To review the literature on intracranial empyema and report two new cases in cats. METHODS: Literature review and case reports. RESULTS: Intracranial empyema has been rarely reported in small animals. In two novel cases in cats, the route of infection was postulated to be local extension from a retrobulbar abscess of odontogenic origin in one case and direct inoculation from a penetrating bite wound to the skull, confirmed at post-mortem examination, in the other. On magnetic resonance imaging of the first case, there was a contrast-enhancing large extra-axial fluid collection overlying the right cerebral hemisphere, consistent with subdural empyema. Infection was caused by an Actinomyces spp. This is the first report of successful treatment of intracranial empyema by craniotomy, drainage and antibiotics. CLINICAL SIGNIFICANCE: Intracranial empyema is a neurosurgical emergency. Favourable outcomes may be achieved with surgical decompression, antimicrobial therapy and intensive care.

Excision of a locally invasive thymoma causing cranial vena caval syndrome in a dog.

A 9-year-old female Golden Retriever was examined because of inappetance, labored breathing, edema, and distension of the veins of the neck. Thoracic radiography revealed pleural effusion and a cranial mediastinal mass. Biopsy results obtained by use of fine-needle aspiration were consistent with thymoma. At surgery, the tumor was found to have invaded the cranial vena cava. Extra- and intravascular portions were removed without complications, and the dog's clinical signs resolved. To our knowledge, this is the first documented report of an invasive thymoma causing cranial vena caval syndrome that has been successfully treated in a dog. In this instance, the simplest surgical method, namely venotomy and tumor extraction using venous inflow occlusion, was successful, obviating the need for temporary or permanent vascular conduits or grafts. These findings indicate that there is potential for surgical correction of invasive thymoma with cranial vena caval syndrome in some animals, and the prognosis is not always poor.

Hepatic carcinoid, hypercortisolism and hypokalaemia in a dog.

A German Shepherd dog was diagnosed with periodic myopathy secondary to persistent hypokalaemia. Hormone analysis revealed excess cortisol secretion. A neuroendocrine carcinoma, thought to be a primary hepatic carcinoid, was detected in the liver. Ectopic adrenocorticotrophin hormone secretion was suspected as the cause of hypercortisolism and hypokalaemia, although this could not be confirmed by immunohistochemical staining.

Chiari 1/syringomyelia complex in a King Charles Spaniel.

A 9-year-old King Charles Spaniel presented with a history of progressive forelimb weakness and paroxysmal involuntary flank scratching over a 2-year period. Neurological examination suggested a myelopathy of C1 to C4 spinal cord segments. Advanced imaging studies revealed hydrocephalus, caudal herniation of part of the caudal lobe of the cerebellum through the foramen magnum and marked syrinx formation to the level of the caudal thoracic spine, resembling Arnold-Chiari malformation with secondary hydromyelia in humans. Mechanical obstruction at the craniocervical junction, altering CSF flow dynamics, may lead to syrinx formation. Response to diuretic therapy was moderate but surgical decompression may offer better long term prognosis.

Canine histiocytic ulcerative colitis.

OBJECTIVE: To assess prevalence, breed predilection, response to therapy and prognosis of canine histiocytic ulcerative colitis (CHUC). DESIGN: A retrospective study of cases of CHUC seen at Sydney University Veterinary Teaching Hospital (SUVTH) over a 20-year period (1975-1994). PROCEDURE: Case records of all dogs in which colitis was suspected were reviewed. Dogs were diagnosed with CHUC based on colonorectal biopsy and histopathological examination. RESULTS: CHUC was diagnosed in 8 of 57 dogs presented for colitis. All affected dogs were Boxers and six were female. Dogs with milder clinical signs showed moderately good response to therapy. Four dogs were still alive 1 to 7 years after diagnosis. Three dogs were euthanased, one for reasons other than CHUC, and one was lost to follow-up. CONCLUSIONS: Young boxer dogs with relatively mild signs of CHUC may respond moderately well to medical and dietary therapy with fair prognosis. Euthanasia early in the course of the disease may be unwarranted. Prevalence may be increasing within the SUVTH referral population.

Immune-mediated neutropenia suspected in five dogs.

Five cases of suspected immune-mediated neutropenia in dogs are described. Clinical signs varied depending on whether the animals had a systemic infection or concurrent immune-mediated disease. Patients were diagnosed by excluding other causes of neutropenia, supportive bone marrow aspirate findings, an initial favourable response to corticosteroid administration in four of the cases, and concurrent immune-mediated disease. Four of the dogs were receiving medications at the time of diagnosis, and immune-mediated neutropenia secondary to drug therapy cannot be excluded. This study shows that appropriate immunosuppressive treatment can lead to a favourable outcome, however, care is required to avoid adverse effects associated with corticosteroid use. It is also imperative that medications are not withdrawn abruptly as a second remission may not always be achievable.

Perirenal pseudocysts in 26 cats.

OBJECTIVE: To evaluate clinical features, anatomical location, nature of pseudocyst fluid, results of surgical treatment and links with underlying renal disease in cats with perirenal pseudocysts. DESIGN: A retrospective study of 26 affected cats, including 8 treated surgically. RESULTS: Nineteen (73%) affected cats were male. The median age was 11 years. Most presented for abdominal enlargement and had varying degrees of renal dysfunction on presentation. Thirteen cats (50%) had bilateral pseudocysts. The pseudocyst fluid was a transudate or modified transudate in all cases. All surgically treated cats had subcapsular perirenal pseudocysts. Associated renal lesions were identified in all cats that had renal biopsies or detailed ultrasonographic examinations. Surgery relieved clinical signs but did not stop progression of renal disease. Cats survived a median of 9 months after surgery and survival was correlated statistically to degree of azotaemia at presentation. Percutaneous drainage of pseudocysts was ineffective in controlling long-term fluid accumulation. CONCLUSIONS: Subcapsular perirenal pseudocysts are formed in cats by accumulation of transudate between the capsule and parenchyma of the kidney as a result of underlying parenchymal disease. Pseudocyst formation can occur at variable stages of renal dysfunction. Resection of the pseudocyst wall is usually effective in eliminating signs but does not stop progression of renal disease. The prognosis for cats with pseudocyst formation is related to the degree of renal dysfunction at time of diagnosis.

Bronchial stent placement in a dog with bronchomalacia and left atrial enlargement.

A 13-year-old neutered male Maltese was referred for paroxysms of coughing and cyanosis, with radiographic evidence of bronchial disease and cardiomegaly. Investigation with echocardiography, bronchoscopy, fluoroscopy and bronchoalveolar lavage led to a diagnosis of myxomatous mitral valve degeneration with insufficiency, ISACHC class II heart failure and bronchomalacia with severe left mainstem bronchial collapse. Persistence of intractable cough despite medical therapy prompted placement of a stent in the left mainstem bronchus. Immediately after stent placement, severe pulmonary oedema developed, thought to be due to compression of the left atrium by the stent or acute lung injury related to stent placement. The dog recovered over a 3-day period with diuretic therapy and positive end expiratory pressure ventilation. Subsequently, the dog died from congestive heart failure 102 days after stent placement, during which time occasional, self limiting coughing episodes occurred.

Intraoperative parathyroid hormone concentration to confirm removal of hypersecretory parathyroid tissue and time to postoperative normocalcaemia in nine dogs with primary hyperparathyroidism.

OBJECTIVE: To determine (1) whether the intraoperative parathyroid hormone concentration ([PTH]) during parathyroidectomy (PTX) can be used to indicate cure in dogs with primary hyperparathyroidism and (2) the time taken for postoperative serum calcium concentration to normalise. DESIGN: Retrospective study (2005-10) from a private referral hospital in Sydney, New South Wales, Australia. PROCEDURE: Nine client-owned dogs underwent surgical PTX for naturally occurring primary hyperparathyroidism. [PTH] was measured from serum samples taken immediately post-induction (pre-PTX]) and at least 20 min after adenoma removal (post-PTX) for all dogs, and during parathyroid gland manipulation (intra-PTX) for six dogs. The concentration of ionised calcium (iCa) was measured at various time points postoperatively until it normalised, then stabilised or decreased below reference ranges. Statistical analysis compared the mean pre-, intra- and post-PTX [PTH] and the average rate of decline of iCa concentration postoperatively. RESULTS: All dogs demonstrated a significant decrease from mean pre-PTX [PTH] (168.51 pg/mL) to mean post-PTX [PTH] (29.20 pg/mL). There was a significant increase in mean intra-PTX [PTH] (279.78 pg/mL). The average rate of decline of iCa concentration postoperatively to within the reference range (1.12-1.40 mmol/L) occurred after 24 h. CONCLUSION: Intraoperative measurements of [PTH] can be used clinically to determine cure of primary hyperparathyroidism. Parathyroid hormone increases significantly during parathyroid gland manipulation. Plasma iCa concentration returns to within the reference range on average 24 h after successful PTX. Not all dogs require vitamin D or calcium supplementation pre- or postoperatively.

Suspected myelinolysis following rapid correction of hyponatremia in a dog.

A dog developed signs of neurological dysfunction five days after rapid correction of severe electrolyte derangements, including hyponatremia, caused by gastrointestinal parasitism (i.e., trichuriasis). History, laboratory findings, and onset of neurological signs following correction of hyponatremia led to a diagnosis of myelinolysis. Myelinolysis is a noninflammatory, demyelinating brain disease caused by sudden, upward osmotic shifts in central nervous system plasma, often a result of rapid correction of chronic hyponatremia. The pathogenesis is complex, but recovery is possible. Iatrogenic damage due to myelinolysis can be avoided by adherence to therapeutic guidelines for correction of chronic hyponatremia.